Induction of epithelial to mesenchymal transition in HPV16 E6/E7 oncogene transfected C33A cell line

Chakraborti, Sourangshu; Karmakar, Aparajita; Guha, Riana; Ngan, Christopher C.; Das, Raunak Kumar; Whitaker, Noel J.

doi:10.1016/j.tice.2023.102041

Cited by 1 publication

(1 citation statement)

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“…Further studies on the regulatory effects of HPV on Wnt/β-catenin signaling indicate that HPV E6 and E7 oncoproteins stabilize β-catenin proteins in the cytoplasm by inhibiting the degradation complex of β-catenin and PP2A in cancer cells [ 95 ]. Additionally, the E6 facilitates the nuclear translocation of β-catenin and induces the expression of Wnt signaling downstream target genes like cyclin D1 and c-MYC, leading to cell growth and proliferation [ 96 ]. Recent studies on the Wnt signaling effects on reducing immune responses against HPV-induced cancer cells indicate that c-MYC upregulates PDL1 on the surface of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Emerging paradigms: unmasking the role of oxidative stress in HPV-induced carcinogenesis

Letafati,

Taghiabadi,

Zafarian

et al. 2024

Infect Agents Cancer

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The contribution of the human papillomavirus (HPV) to cancer is significant but not exclusive, as carcinogenesis involves complex mechanisms, notably oxidative stress. Oxidative stress and HPV can independently cause genome instability and DNA damage, contributing to tumorigenesis. Oxidative stress-induced DNA damage, especially double-strand breaks, aids in the integration of HPV into the host genome and promotes the overexpression of two viral proteins, E6 and E7. Lifestyle factors, including diet, smoking, alcohol, and psychological stress, along with genetic and epigenetic modifications, and viral oncoproteins may influence oxidative stress, impacting the progression of HPV-related cancers. This review highlights various mechanisms in oxidative-induced HPV-mediated carcinogenesis, including altered mitochondrial morphology and function leading to elevated ROS levels, modulation of antioxidant enzymes like Superoxide Dismutase (SOD), Glutathione (GSH), and Glutathione Peroxidase (GPx), induction of chronic inflammatory environments, and activation of specific cell signaling pathways like the Phosphoinositide 3-kinase, Protein kinase B, Mammalian target of rapamycin (PI3K/AKT/mTOR) and the Extracellular signal-regulated kinase (ERK) signaling pathway. The study highlights the significance of comprehending and controlling oxidative stress in preventing and treating cancer. We suggested that incorporating dietary antioxidants and targeting cancer cells through mechanisms involving ROS could be potential interventions to mitigate the impact of oxidative stress on HPV-related malignancies.

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Section: Introductionmentioning

confidence: 99%